Subcutaneous injection of bee venom causes long-term neural activation and hypersensitization in the dorsal horn of the spinal cord,which contributes to the development and maintenance of various pain-related behavior...Subcutaneous injection of bee venom causes long-term neural activation and hypersensitization in the dorsal horn of the spinal cord,which contributes to the development and maintenance of various pain-related behaviors.The unique behavioral 'phenotypes' of nociception and hypersensitivity identified in the rodent bee venom test are believed to reflect a complex pathological state of inflammatory pain and might be appropriate to the study of phenotype-based mechanisms of pain and hyperalgesia.In this review,the spinal processing of the bee venom-induced different 'phenotypes' of pain and hyperalgesia will be described.The accumulative electrophysiological,pharmacological,and behavioral data strongly suggest that different 'phenotypes' of pain and hyperalgesia are mediated by different spinal signaling pathways.Unraveling the phenotype-based mechanisms of pain might be useful in development of novel therapeutic drugs against complex clinic pathological pain.展开更多
Objective To examine whether microinjection of morphine into the rat thalamic nucleus submedius (Sm) could depress the bee venom (BV)-induced nociceptive behaviours. Methods In inflammatory pain model induced by BV su...Objective To examine whether microinjection of morphine into the rat thalamic nucleus submedius (Sm) could depress the bee venom (BV)-induced nociceptive behaviours. Methods In inflammatory pain model induced by BV subcutaneous injection into rat unilateral hind paw,the inhibitory effects of morphine microinjection into thalamic nucleus submedius (Sm) on the spontaneous nociceptive behavior,heat hyperalgesia and tactile allodynia,and the influence of naloxone on the morphine effects were observed in the rat. Results A single dose of morphine (5.0 μg,0.5 μL) applied into the Sm ipsilateral to the BV injected paw significantly depressed the spontaneous paw flinching response. Morphine also significantly increased the heat paw withdrawal latencies in the bilateral hind paw and the tactile paw withdrawal threshold in the ipsilateral hind paw 2 hours after BV injection. All these depressive effects could be effectively antagonized by pre-treatment with the opioid receptor antagonist naloxone (1.0 μg,0.5 μL) in the Sm 5min prior to morphine administration. Naloxone alone injected to the Sm had no effect on the BV-induced nociceptive behavior. Conclusion These results suggest that Sm is involved in opioid receptor-mediated anti-nociception in the rat with the BV-induced inflammatory pain. Together with results from previous studies,it is likely that this effect is produced by activation of the Sm-ventrolateral orbital cortex-periaqueductal gray pathway,leading to activation of the brainstem descending inhibitory system and depression of the nociceptive inputs at the spinal cord level.展开更多
基金grants from National Natural Science Foundation of China(No.30325023,30670692)Natural Science Foundation of Beijing Education Committee(No.KZ200510025016)+1 种基金National Basic Research Development Program(973)of China(No.2006CB500808)Innovation Research Team Program of Ministry of Education,China(No.IRT0560)
文摘Subcutaneous injection of bee venom causes long-term neural activation and hypersensitization in the dorsal horn of the spinal cord,which contributes to the development and maintenance of various pain-related behaviors.The unique behavioral 'phenotypes' of nociception and hypersensitivity identified in the rodent bee venom test are believed to reflect a complex pathological state of inflammatory pain and might be appropriate to the study of phenotype-based mechanisms of pain and hyperalgesia.In this review,the spinal processing of the bee venom-induced different 'phenotypes' of pain and hyperalgesia will be described.The accumulative electrophysiological,pharmacological,and behavioral data strongly suggest that different 'phenotypes' of pain and hyperalgesia are mediated by different spinal signaling pathways.Unraveling the phenotype-based mechanisms of pain might be useful in development of novel therapeutic drugs against complex clinic pathological pain.
基金supported by the National Natural Science Foundation of China (No.3027045330570592)
文摘Objective To examine whether microinjection of morphine into the rat thalamic nucleus submedius (Sm) could depress the bee venom (BV)-induced nociceptive behaviours. Methods In inflammatory pain model induced by BV subcutaneous injection into rat unilateral hind paw,the inhibitory effects of morphine microinjection into thalamic nucleus submedius (Sm) on the spontaneous nociceptive behavior,heat hyperalgesia and tactile allodynia,and the influence of naloxone on the morphine effects were observed in the rat. Results A single dose of morphine (5.0 μg,0.5 μL) applied into the Sm ipsilateral to the BV injected paw significantly depressed the spontaneous paw flinching response. Morphine also significantly increased the heat paw withdrawal latencies in the bilateral hind paw and the tactile paw withdrawal threshold in the ipsilateral hind paw 2 hours after BV injection. All these depressive effects could be effectively antagonized by pre-treatment with the opioid receptor antagonist naloxone (1.0 μg,0.5 μL) in the Sm 5min prior to morphine administration. Naloxone alone injected to the Sm had no effect on the BV-induced nociceptive behavior. Conclusion These results suggest that Sm is involved in opioid receptor-mediated anti-nociception in the rat with the BV-induced inflammatory pain. Together with results from previous studies,it is likely that this effect is produced by activation of the Sm-ventrolateral orbital cortex-periaqueductal gray pathway,leading to activation of the brainstem descending inhibitory system and depression of the nociceptive inputs at the spinal cord level.
